Galectin-3 and ST2 are emerging biomarkers involved in myocardial fibrosis. We evaluate the relevance of a multiparametric biomarker approach based on increased serum levels of NT-proBNP, galectin-3, and ST2 in stratifying the prognosis of chronic heart failure (CHF) outpatients. In 315 CHF outpatients in stable clinical condition clinical and echocardiographic evaluations were performed. Routine chemistry and serum levels of NT-proBNP, galectin-3, and ST2 were also assessed. During a 12 month follow-up, cardiovascular death, and/or heart failure (HF) occurred in 64 patients. The presence of NT-proBNP, galectin-3, and ST2 were higher than the recommended cutoffs and were all associated with events at univariate Cox regression analysis, as well as in a multivariate analysis including the three biomarkers. When a score based on the number of biomarkers above the recommended cut-offs was used (in a range of 0–3), it was associated with events both with respect to the univariate (HR 2.96, 95% CI 2.21–3.95, p < 0.001, C-index 0.78) and the multivariate (HR 1.52, 95% CI 1.06–2.17, p: 0.023, C-index 0.87) analyses, after correction for the variables of a reference model. Our results suggest that an easy prognostic approach based on the combination of three biomarkers, although with partially-overlapping pathophysiological mechanisms, is able to identify patients with the highest risk of heart failure progression.

Aim: The aim of the study was to evaluate the association between Gal-3 serum levels and the progression of renal dysfunction in chronic heart failure outpatients. Methods & results: This prospecti...

Cancer-associated thrombosis (CAT) is a devastating complication of cancer that can significantly impact a patient’s health and life. The incidence of CAT is approximately 20%, and 1 in 5 cancer patients will develop CAT annually. Indeed, CAT can promote pulmonary embolism and deep vein thrombosis, leading to increased morbidity and mortality that dramatically impact survival. CAT can also provoke delay or discontinuation of anticancer treatment, which may result in a lack of treatment efficacy and high costs for patients, institutions, and society. Current guidelines advocate direct oral anticoagulants (DOACs) as the first-line anticoagulant option in CAT. Compared to low-molecular-weight-heparins (LMWHs), DOACs are advantageous in that they typically have an oral route of administration, do not require laboratory monitoring, and have a more predictable anticoagulant effect. However, in patients with thrombocytopenia, renal failure, or those receiving anticancer regimens with potential for drug-drug interactions, LMWH is still the mainstay of care. The main limitation of current anticoagulant agents is related to bleeding risk (BR), both for DOACs and LMWHs. Specifically, DOACs have been associated with high BR in gastrointestinal and genitourinary cancers. In this challenging scenario, abelacimab, an anti-factor XI agent, could represent a viable option in the management of CAT due to its “hemostasis sparing” effect. The safe profile of abelacimab could be useful in patients with active malignancy and CAT, as long-term anticoagulant therapy is often required. Two ongoing international phase III trials (Aster and Magnolia) compare abelacimab with the standard of care (i.e., apixaban in patients with CAT and dalteparin in those with CAT and high BR, respectively). Abelacimab is a new and attractive anticoagulant for the management of CAT, especially in the insidious and critical scenario of active cancer patients with venous thromboembolism and high BR. The aim of this narrative review is to discuss the updated evidence on the performance of DOACs and LMWHs in the treatment of CAT and to focus on the potential role of abelacimab in CAT and its promising associated clinical trials.

Cancer‐associated thrombosis (CAT) is the second main cause of cancer death with high related mortality and morbidity, leading to anticancer agent delays and interruptions. The recommended therapy, low‐molecular‐weight heparin (LMWH), however, is burdensome for patients and costly for society, as treatment should last until cancer is no longer active, even indefinitely. Tinzaparin is a manageable, efficient, safe, and cost‐effective option. Compared to the other LMWHs, advantages are single‐daily dose and safety in the elderly and those with renal impairment (RI). The purpose of this review is to critically discuss recent data on its efficacy and safety in CAT.

Rationale: Venous thromboembolism is a feared frequent complication of cancer with a 2-way relationship. Low molecular weight heparin is the mainstay of treatment. The use of direct oral anticoagulants is supported by established evidence for the treatment of deep vein thrombosis also in active cancer and they are prioritized over low molecular weight heparin for cancer-associated thrombosis according to current guidelines. However, upper limb deep vein thrombosis is poorly studied with scant data on the use of direct oral anticoagulants in noncatheter-related deep vein thrombosis. We report the case of a patient with noncatheter-related deep vein thrombosis and a rare tumor site effectively and safely treated with a direct oral anticoagulant, edoxaban, after lack of efficacy with low molecular weight heparin. Patient concerns: A 35-year-old man with primitive mediastinal seminoma presented at our Cardio-Oncology Unit for prechemotherapy assessment. Diagnosis: Persistent brachiocephalic deep vein thrombosis, despite full-dose enoxaparin, was detected at ultrasonography. Intervention: We decided to switch the anticoagulant treatment from enoxaparin to edoxaban. Outcome: The 3-month ultrasonography showed almost total regression of the deep vein thrombosis without any adverse effects and a good patient compliance. Lessons: We conducted a literature review on upper limb deep vein thrombosis, since its management is challenging due to inconsistency of evidence. This report highlights the benefits of direct oral anticoagulants compared to low molecular weight heparins in cancer-associated thrombosis therapy in terms of efficacy, safety and ease of use.

Background: Hypothyroidism and low T3 syndrome frequently occur in HF patients. Aim of the study: To evaluate in a large sample of CHF patients the association between thyroid hormone deficiencies and poor outcome. Methods and results: From 2006 to 2015, we screened 712 consecutive CHF outpatients (551 males, 64±14 years, left ventricular ejection fraction (LVEF) 33±10%, NYHA class 2.3±0.6, NTproBNP 2153±4696 pg/ml, GFR-EPI 71±25 ml/min*1.73 m²) in stable clinical conditions (>1 month) and in conventional therapy. All patients underwent assessment of thyroid function. A total of 34 patients were excluded for hyperthyroidism; among the remaining 678, 58 (9%) showed a TSH level above the upper normal limit, but below 10 microU/ml, 23 (3%) a TSH value above 10 microU/mL, and 20 patients (3%) low fT3 (LT3) levels without changes in TSH levels. During a mean follow-up of 38 months, 122 patients died (101 for cardiovascular causes) and 202 experienced at least one admission for acute decompensated heart failure. TSH >10 microU/mL (HR:2.96; 95%CI: 1.54–5.68; P: 0.001) and LT3 (HR: 3.79; 95%CI: 1.91–7.54; P<0.001), but not high TSH<10 microU/mL (HR: 1.59; 95%CI: 0.871–2.91; P: 0.13), were associated with an increased risk of death at univariate analysis. At multivariate Cox regression analysis, after correction for the presence of NYHA class 3, LVEF1000, systolic arterial pressure <100 mm Hg and GFR-EPI <60 ml/min, only LT3 remained significantly associated with events (HR: 2.75; 95%CI:1.38–5.49; P: 0.004). When the occurrence of heart failure hospitalization was considered, high TSH levels with a value <10 microU/ml (HR 1.82; 95% CI: 1.18–2.83; P10 microU/ml (HR 2.84; 95%CI:1.61–5.01; P<0.001) and LT3 (HR: 3.33; 95%CI: 1.89–5.88; P10 microU/ml (HR: 1.91; 95%CI:1.06–3.46; P:0.03) and LT3 (HR: 2.39; 95%CI: 1.36–4.24; P:0.002), but not high TSH with value <10 microU/ml, remained associated with HF hospitalization. Conclusions: In this observational study on a large cohort of CHF outpatients, we found that impaired thyroid function, particularly when high levels of TSH (>10 microUI/ml) and low T3 levels are considered, has an independent adverse impact on CHF events.